The purpose of the research to be conducted is to determine the mechanism for cataracts formed in rat lenses by administration of elevated amounts of the trace mineral selenium. These major areas of lenticular function will be investigated: a) energy supply (lens and blood glucose levels), b) electrolyte balance and the integrity of the cation pump (Na, K, H2O, and Na-K dependent ATPase assays), c) status of the lenticular proteins whose physical-chemical properties may determine cataractogenesis (total proteins, proportions of soluble and insoluble proteins), d) integrity of the oxido-reductase protective enzymes (glutathione peroxidase, catalase, and superoxide dismutase), e) correlation of selenium uptake into the lens with cataract and biochemical changes and changes in lenticular selenium concentrations with time, and f) ultrastructural changes of the lens (transmission electron microscopy). These measurements will be made both in lenses of rats receiving selenite (causes cataracts) and in rats receiving selenomethionine (does not cause cataracts) as well as controls. Using these two forms of selenium, we should be further able to differentiate which changes are important to cataractogenesis and which changes, although associated with selenium intake, are not important to cataractogenesis. Experiments will also be performed to determine: a) the chemical forms of selenium in the lens, b) histological characteristics of transient selenium cataracts, c) efficacy of alimentary versus injected selenium in cataractogenesis, d) the mechanism of possible amelioration of selenium induced cataract by cadmium, and e) the mechanism for the lack of cataractogenesis by selenium in the hamster. We hope our studies will provide a well defined animal model for cataracts (possibly induced by oxygen metabolite toxicity) which may be relevant to the prevention or treatment of human senile cataract.